Document Detail


P/Q-type calcium channel ablation in a mice glycinergic synapse mediated by multiple types of Ca²+ channels alters transmitter release and short term plasticity.
MedLine Citation:
PMID:  21718757     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ca(v)2.1 channels (P/Q-type) play a prominent role in controlling neurotransmitter release. Transgenic mice in which the α1A pore-forming subunit of Ca(v)2.1 channels is ablated (KO) provide a powerful tool to study Ca(v)2.1 function in synaptic transmission in vivo. Whole-cell patch clamp was used to measure inhibitory glycinergic postsynaptic currents (IPSCs) from the lateral superior olive (LSO). Comparing wild-type (WT) and KO mice, we investigated the relevance of P/Q-type calcium channels at a glycinergic synapse mediated by multiple types of Ca(2+) channels, in opposition to synapses where only this type of Ca(2+) channels are in charge of transmitter release. We found that in KO mice, N-type and L-type Ca(2+) channels control synaptic transmission, resulting in a functional but reduced glycinergic transmitter release. Pair pulse facilitation of synaptic currents is retained in KO mice, even when synaptic transmission is driven by either N or L-type calcium channels alone, in contrast with lack of this phenomenon in other synapses which are exclusively mediated by P/Q-type channels. Thus, pointing a difference between P/Q- and N-type channels present in single or multiple types of calcium channels driven synapses. Significant alterations in short-term synaptic plasticity were observed. KO mice exhibited a stronger short term depression (STD) of IPSCs during repetitive stimulation at high frequency and recovered with a larger time constant compared to WT mice. Finally, transmitter release at the LSO synapse from KO mice was strongly modulated by presynaptic GTP-binding protein-coupled receptor γ-aminobutyric acid type B (GABA(B)).
Authors:
B Giugovaz-Tropper; C González-Inchauspe; M N Di Guilmi; F J Urbano; I D Forsythe; O D Uchitel
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-06-14
Journal Detail:
Title:  Neuroscience     Volume:  192     ISSN:  1873-7544     ISO Abbreviation:  Neuroscience     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-09-02     Completed Date:  2012-01-18     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  United States    
Other Details:
Languages:  eng     Pagination:  219-30     Citation Subset:  IM    
Copyright Information:
Copyright © 2011. Published by Elsevier Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain Stem / metabolism
Calcium Channels / metabolism
Calcium Channels, P-Type / metabolism*
Calcium Channels, Q-Type / metabolism
Excitatory Postsynaptic Potentials / physiology
Glycine / metabolism
Inhibitory Postsynaptic Potentials / physiology
Mice
Mice, Knockout
Mice, Transgenic
Neuronal Plasticity / physiology*
Neurons / metabolism
Neurotransmitter Agents / secretion*
Organ Culture Techniques
Patch-Clamp Techniques
Synapses / metabolism*
Synaptic Transmission / physiology*
Grant Support
ID/Acronym/Agency:
MC_U132681855//Medical Research Council; RM36 046//Wellcome Trust
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Calcium Channels, P-Type; 0/Calcium Channels, Q-Type; 0/Neurotransmitter Agents; TE7660XO1C/Glycine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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